Skeletal trauma and other serious illnesses result in the excessive loss of skeletal muscle protein. This loss of protein becomes life threatening if allowed to continue for an extended period. It is hypothesized that the increased oxidation of the branched-chain amino acids; leucine, valine, and isoleucine; is a major contributor to the protein wasting state. In this study the oxidation of the branched-chain amino acid, leucine, by the traumatized rat was investigated. The trauma model was bilateral femoral fracture with intravenous total parenteral nutrition assuring similar dietary intake for all animals. Preliminary studies showed that switching from D5W as the only nutritional support to TPN stimulated the amount of the leucine dose oxidized in four hours from 27% to 32%. Large rats (300-350g) were found to oxidize 20% more of the leucine dose in 4 hours than did smaller animals (150-200g). The investigation of leucine oxidation in traumatized rats has demonstrated a correlation between leucine oxidation and urinary nitrogen excretion. The traumatized rats, compared to controls, demonstrated an increase in urinary nitrogen that peaks on the second day and is falling toward normal by the third day post-trauma. Leucine oxidation also appears to go through a peak on the second day. The traumatized animals do not display an increase in leucine oxidation of the same magnitude as we have reported for humans. The data from rats suggest that the trauma is not as severe as found in man but that the catabolic response is present.